It is claimed E. coli may have been a benign bacteria in earlier times when scientists didn't play at being God. However, in those earlier times it wasn't called E. coli. It was called Bacillus coli communis and it could be just as deadly Later it was discovered that E. coli DNA could be manipulated to produce drugs, pesticides, fuel, etc.

After 12 brain surgeries, UK boy recovers from battle with E. coli15.dec.11barfblogBen Chapmanhttp://barfblog.com/blog/152002/11/12/15/after-12-brain-surgeries-uk-boy-recovers-battle-e-coliWith two boys under four, I get pretty emotional when I read a story about a child getting sick from food borne illness. This week Jack had a cold, and I felt helpless when he said "make me feel better." I can't imagine what Thomas Miller's parents felt like over the past two years as they saw him battling the effects of E. coli infection complications which included a septicemia and rare brain impacts. Thomas' illness was linked to eating contaminated burgers and is being reported as the first time an individual in the UK has recovered from these complications. The youngster, who was two-years-old at the time, fell ill just 24 hours after eating a beef burger on a family day out in Scotland in 2009.His older brother James, then seven, suffered diarrhoeaand a day later Thomas started to pass blood.‘We just didn’t know what was happening. It was frightening,’ said 37-year-old Mrs Miller, from Aspatria,Cumbria. ‘He went for an operation that day and had to have dialysis. ‘He was holding his head and screaming, he couldn’t move and was as stiff as a board.’ The E.coli had entered Thomas’ bloodstream but further scans revealed it was also attacking his brain. Two golf ball-sized abscesses on his brain, which had caused him to go blind, were drained in August 2009 – allowing him to see again. But his ordeal wasn’t over as he developed more abscesses on the brain and even suffered an allergic reaction to the medication, which ‘burned’ his skin. Finally last year, after having all the abscesses removed, he was given the all clear. ‘I’ll never forget the day he came out of intensive care,’ said Mrs Miller. ‘It’s only really this year that I’ve been able to relax.’

EPA's scientists seems to have missed the fact that even the least virulent E. coli can be a killer. Outsidethe stomach and colon, the endogenous coliform E. coli, with no virulence factors, have beenimplicated in respiratory tract infections such as pneumonia, blood poisoning (septicaemia), endotoxicshock, high blood pressure, scarring and eventually kidney failure, mental changes or confusion,neonatal meningitis, and urinary tract infections leading to serious infections of the prostate(prostatitis), bladder, and kidneys (pyelonephiritis) and death. According to Palomar CollegeMicrobiology Instructor, Ana Dowey, “50 to 80% of urinary tract infections in healthy people areproduced by self-contamination from endogenous strains of E. coli.” E. coli, with no virulence factors.This is called an opportunistic pathogen. That also means 20 to 50% of the urinary tract infectionscould be from taking a bath in E. coli contaminated tap water.

Before E. coli took on Theodor Escherich's name, it was one of the first documented bacterial killers.By 1903, Scientists like William Savage MD were well aware that there were varying virulence levelsbetween members of Bacillus coli (B. coli). However, he was of the opinion that only exposure to B.coli from humans was of concern in drinking water. His wish was to have a test that separated humanB. coli from environmental strains of similar coli forms of bacteria. http://www.jstor.org/pss/3858994

In 1904, Christiaan Eijkman discovered some strains of E. coli could grow above 112.1°F. He claimedthe higher temperature differentiated them from environmental strains which scientists agreed had nosanitary significance. This strain of thermotolerant E. coli assumed the name fecal coliform. E. colistrains that grew at optimum growth temperature of 98.6°F were named coliform by the Public HealthService in 1914 and also considered to have no sanitary significance. It is amazing that after onehundred and seven years some scientists still believe the myth. Yet, the medical profession has alwayshad a different view of what was then called Coli bacillus or Bacillus coli and tested it at normal bodytemperature.

In the 1910 article, “Discussion On Infections Of The Urinary Tract By Bacillus Coli In Infancy AndChildhood,” Charles R. Box, et al., reported the progression of the infections in infants and youngchildren, including death. http://www.jstor.org/pss/25292509

In the 1919 edition of “Modern Surgery” John Chalmers Da Costa, stated, “This bacillus may beresponsible for appendicitis, peritonitis [thin tissue that lines the inner wall of the abdomen and coversmost of the abdominal organs], inflammation of the genito-urinary tract, pneumonia, inflammation ofthe intestine, leptomeningitis [form of meningitis which complicates the course of all of the acuteinfections], perineal abscess [between vaginal opening and rectum], cholangitis [infection of thecommon bile duct], cholecystitis [bacterial infection superimposed on an obstruction of the biliarytree], myelitis [inflammation of the spinal cord], puerperal fever [bacterial infection contracted bywomen during childbirth or miscarriage], wound infections and septicemia [bacteria contaminating theblood]. It is the cause of many abscesses about the intestine and responsible for many ischiorectalabscesses [region between the rectum and ishial tuberosity – sitz bone].”

In the 1921 study “ON BACILLUS COLI INFECTIONS OF THE URINARY TRACT, ESPECIALLYIN RELATION TO HAEMOLYTIC ORGANISMS,” according to Leonard S. Dudgeon,“A great point has been made by those who believe that all urinary infections are primarily via theblood stream in that the B. coli can be obtained in pure culture from the blood, but the fact that suchbacilli may be so recovered does not point to the origin of the infection, since in view of Thiele andEmbleton's experiments, even if the colon bacillus did start from the urethral mucous membrane itwould still be found in the blood. A careful examination of the blood in B. coli infections of the urinarytract has shown that such bacilli may be isolated very frequently, especially if the blood is taken at theheight of the rigor. Cabot and Crabtree (1916) obtained positive blood cultures in 40 percent of casesout of 32 examined. Conclusion:(1) Bactllus coli in infected urine can be divided into two groups: (i) haemolytic; (ii) non-haemolytic.(2) The haemolytic group is the common type in the infection in men and the non-haemolytic inwomen.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2207040/pdf/jhyg00382-0041.pdf

In the 1984 New England Journal of Medicine article “Mortality Associated with Nosocomial Urinary-Tract Infection,” R. Platt and associates reported that hospital acquired UTIs were deadly. They stated,“Seventy-six patients (25 infected and 51 noninfected) died during hospitalization; death rates were 19per cent in infected patients and 4 per cent in noninfected patients”http://www.nejm.org/doi/full/10.1056/NEJM198209093071101

Urinary tract infections often occur from fecal material getting into the urethra. In 1934 study, Edith E.Nicholls reported on “THE INCIDENCE AND BIOLOGICAL CHARACTERISTICS OF THEHEMOLYTIC BACILLUS COLI IN THE STOOLS OF HEALTHY INDIVIDUALS.” Hemolyticmeans the bacteria break down red blood cells. She found that in appropriate doses, both types ofbacteria killed white mice. Greater numbers of hemolyic bacteria were more likely to be found inpeople with "diarrhea or colitis." However, time and temperature could cause the bacteria to lose thehemolytic capability. According to Nicholls, "Fifty to one hundred per cent of the specimens, from eachindividual, showed hemolytic Bacillus coli." The specific finding was, "The hemolytic strains ofBacillus coli recovered from stool specimens were found to be only slightly more virulent for whitemice than were the nonhemolytic."http://www.jci.org/articles/view/100599

According to EPA, “2% to 7% of children and elderly infected with E. coli [0157;H7], may develophemolytic uremic syndrome, in which the red blood cells are destroyed and the kidneys fail; 33% ofpersons with hemolytic uremic syndrome have abnormal kidney function many years later, and a fewrequire long-term dialysis, a smaller percentage of persons with hemolytic uremic syndrome develophigh blood pressure, seizures, blindness, paralysis, and the effects of having part of their bowelremoved.” http://www.epa.gov/reg3wapd/cso/pdf/CSO_symptoms.pdfIn a 1935 study, “A Study of B. coli mutabile from an Outbreak of Diarrhea in the New-born,” AnnaDean Dulaney, Ph.D., and I. D. Michelson, M.D. of the Medical School at the University of Tennessee,Memphis, reported the first outbreak of B. coli diarrhea among new-born infants in the MemphisGeneral Hospital during the winter of 1933-34. The mortality rate was 47%.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1559361/

Todar's Online Textbook of Bacteriology states, “It was not until 1935 that a strain of E. coli wasshown to be the cause of an outbreak of diarrhea among infants. The GI tract of most warm-bloodedanimals is colonized by E. coli within hours or a few days after birth. The bacterium is ingested infoods or water or obtained directly from other individuals handling the infant. The human bowel isusually colonized within 40 hours of birth. E. coli can adhere to the mucus overlying the large intestine.Once established, an E. coli strain may persist for months or years. Resident strains shift over a longperiod (weeks to months), and more rapidly after enteric infection or antimicrobial chemotherapy thatperturbs the normal flora. The basis for these shifts and the ecology of Escherichia coli in the intestineof humans are poorly understood despite the vast amount of information on almost every other aspectof the organism's existence.” http://textbookofbacteriology.net/e.coli.html

Today, there are more than 200 hydrogen sulfide producing variants of E. coli and an unknown numberof pathogenic chimeric clones including 3,520 unique strains of E. coli 0157:H7 reported to CDCPulseNet between 1996 and 2006. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm55d926a1.htm

The “E. coli Reference Center (formerly Gastroenteric Disease Center) is a part of Animal DiagnosticLaboratory in the Department of Veterinary and Biomedical Sciences” at PennState houses “the largestrepository for E. coli strains in America. It holds more than 70,000 strains collected over the last 50years from animals, humans, birds and environment.” http://ecoli.cas.psu.edu/Since the mid-1970s E.coli has been the work-horse of the genetic engineering researchers. It hasaccepted genes inserted in the laboratory from other bacteria, viruses, yeast, plants and humans,including antibiotic resistant marker genes. Since that time it has become infamous for containing theShiga-toxin genes such as stx1, stx2, rfb and EHEC hlyA (shiga-toxigenic Escherichia coli (STEC))which causes bloody diarrhoea, haemorrhagic colitis (HC) and haemolytic uraemic syndrome (HUS).The use of antibiotics on STEC may cause an immediate release of deadly toxins, and shortlythereafter, death.

In 1989, EPA claimed pathogenic strains of E. coli in “treated” sludge (biosolids) only causedgastroenteritis (diarrhea associated with nausea and vomiting). Even that small warning was removedfrom the final regulation. According to the International Escherichia and Klebsiella Centre (WHO), ithas a very large strain collection of approximately 60,000 E. coli strains, most of which are clinicalisolates. This collection includes test and reference strains for O, K, H and F antigens, various toxinsand other E. coli virulence factors. The collection contains strains representing almost any possiblesero- and virulence type.

2010, Morbidity and Mortality Weekly Report (MMWR), “Detection of Enterobacteriaceae IsolatesCarrying Metallo-Beta-Lactamase --- United States, 2010,” CDC reported, “During January--June2010, three Enterobacteriaceae isolates carrying a newly described resistance mechanism, the NewDelhi metallo-beta-lactamase (NDM-1) (1), were identified from three U.S. states at the CDCantimicrobial susceptibility laboratory. This is the first report of NDM-1 in the United States, and thefirst report of metallo-beta-lactamase carriage among Enterobacteriaceae in the United States. Theseisolates, which include an Escherichia coli, Klebsiella pneumoniae, and Enterobacter cloacae, carryblaNDM-1, which confers resistance to all beta-lactam agents except aztreonam (a monobactamantimicrobial) (1); all three isolates were aztreonam resistant, presumably by a different mechanism. Inthe United Kingdom, where these organisms are increasingly common, carriage of Enterobacteriaceaecontaining blaNDM-1 has been closely linked to receipt of medical care in India and Pakistan (2). Allthree U.S. isolates were from patients who received recent medical care in India.”http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5924a5.htm

E. coli in Animals

E. coli causes colibacillosis in animals. According to the Merk vetmanual, “Colibacillosis occurs as anacute fatal septicemia or subacute pericarditis and airsacculitis. It is a common systemic disease ofeconomic importance in poultry and is seen worldwide.”http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/202000.htm

Baby Calf Health: Common Diarrheal DiseasesColibacillosis usually occurs in calves 1-10 days old. “E. coli organisms are part of the normal flora ofthe intestinal tract. Many strains are harmless to the calf, but certain strains can cause moderate tosevere scours and even death. E. coli typically produces a secretory diarrhea resulting from theintestinal epithelial cells being switched from an absorption mode to a secretion mode. E. coli is oftenreferred to as "white" scours and is the most common cause of calf scours.3 TypesEnteric. This is the most common type. The main clinical sign is severe diarrhea. The calf rapidlybecomes weak and dehydrated with an initial fever that rapidly returns to normal (or subnormal).Dehydration can lead to death.Enterotoxigenic. (K-99 strain) This infection runs a rapid, fatal course. Toxins cause so much fluid tobe pumped into the intestine that the calf usually dies before external signs of diarrhea are present. Thistype of scours is one of the few that occur within the first 3 days of life.Septicemic. This type acts like Salmonella by invading the blood stream and penetrating body tissuescausing a general infection. Gross lesions are usually minimal. This is a rapid form of E. coli, oftenwith no evidence of diarrhea. Colostrum deprived calves usually die of this form of E. coli.1http://www.merricks.com/tech_calfscours.html

As far back as 1891, bacteria was found to cause illness in cows. In the 1891 article,“OBSERVATIONS UPON A MASTITIS BACILLUS.” By ALLAN MACFADYEN, M.D. (Ed.) Hesaid, “In the Agricultural Year-Book of Switzerland for 1888, Professor Hess, of Berne, published theresults of an inquiry into the causes of mastitis in cows. He proved that the infectious forms of mastitisare due to several and distinct kinds of bacteria, which penetrate through the milk canals into the milkglands. Within the latter they find a soil suitable for their growth, and for the development of theirspecific pathogenic properties. The resulting inflammation of the tissues is at times so mild, and thealterations in the secretion so slight, that the affected cows can still be milked, and the milk used fordomestic purposes or for the manufacture of cheese. The milk from one affected cow, by being mixedwith milk from healthy cows, can infect large quantities with the active bacteria. The determination ofthe nature and the action of these bacteria is, therefore, of hygienic and economic importance.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1328128/

In the 2003 study, “S everity of E. coli mastitis is mainly determined by cow factors ,” ChristianBurvenich, et al., Ghent University at Merelbeke, Belgium, reported, “Escherichia coli causesinflammation of the mammary gland in dairy cows around parturition and during early lactation withstriking local and sometimes severe systemic clinical symptoms. This disease affects many highproducing cows in dairy herds and may cause several cases of death per year in the most severe cases.It is well known that bacterial, cow and environmental factors are interdependent and influence mastitissusceptibility. Many studies, executed during the last decade, indicate that the severity of E. colimastitis is mainly determined by cow factors rather than by E. coli pathogenicity. During E. colimastitis, the host defense status is a cardinal factor determining the outcome of the disease. Today, weknow that the neutrophil is a key factor in the cows' defense against intramammary infection with E.coli. Effective elimination of the pathogen by neutrophils is important for the resolution of infectionand the outcome of E. coli mastitis.” https://biblio.ugent.be/input/download?func=downloadFile&fileOId=984758

In the 2009 study, “Human Health Hazards from Antimicrobial-Resistant Escherichia coli of AnimalOrigin,” Anette M. Hammerum, et al., National Center for Antimicrobials and Infection Control,Statens Serum Institut at Copenhagen, reported, “E. coli is a commensal bacterium in the intestine ofpoultry, cattle, and pigs that are used for food production, and food of animal origin can becontaminated with E. coli during slaughter of the animals. E. coli from meat has mostly been associatedwith intestinal pathogenic E. coli (e.g., enteropathogenic, enterotoxigenic, and verotoxigenic E. coli),but recently, E. coli of animal origin has been shown to also be associated with extra-intestinalinfections, such as urinary tract infections. In humans, the majority of infections caused by E. coli arenot harmful (e.g., uncomplicated urinary tract infections), whereas other infections (e.g., blood streaminfections) may be lethal. In many cases, the origin of E. coli that cause infection in humans remainsunknown, and the significance of the animal reservoir of antimicrobial-resistant E. coli has not beenquantified.” http://cid.oxfordjournals.org/content/48/7/916.full

In the 2011 Virginia Cooperative Extension bulletin, “Escherichia coli: A Practical Summary forControlling Mastitis,” Christina S. Petersson-Wolfe, Assistant Professor, Dairy Science, Virginia Tech,and John Currin, Assistant Professor, Virginia-Maryland Regional College of Veterinary Medicine,reported, "... the control of environmental pathogens still remains a daunting task. Escherichia coli areGram-negative bacteria, similar in structure to Klebsiella spp. E. coli mastitis is typically associatedwith a quick onset and often severe clinical signs. -- These organisms are commonly found in organicmatter including bedding and manure. -- E. coli will infect mammary glands through environmentalcontact. -- When E. coli bacteria die, a toxin is released; this toxin is the primary cause of the clinicalsigns observed in a local mastitis infection. Antibiotics act to kill bacteria and in the case of theseinfections, would then result in the toxin release. Therefore, intramammary antibiotic treatment is not agenerally recommended practice for local infections.” http://pubs.ext.vt.edu/404/404-224/404-224.htmlIn the 2011 bulletin, “Control of E. coli mastitis starts with vaccination,” Pfizer Animal Health, said,“Research shows 60 percent to 70 percent of coliform mastitis infections become clinical.1 Coliformmastitis, when it occurs, can become severe and cause these negative impacts on your cows:FeverAbnormal milkExcessive udder edemaDramatic drop in milk productionDeath”http://www.dairyherd.com/dairy-resources/mastitis/Control-of-E-coli-mastitis-starts-with-vaccination-126774653.htm

E. coli in Plants

In a 2002 study, “”Transmission of Escherichia coli O157:H7 from Contaminated Manure andIrrigation Water to Lettuce Plant Tissue and Its Subsequent Internalization, Ethan B. Solomon, et al.,Rutgers University at New Brunswick, reported, “The transmission of Escherichia coli O157:H7 frommanure-contaminated soil and irrigation water to lettuce plants was demonstrated using laser scanningconfocal microscopy, epifluorescence microscopy, and recovery of viable cells from the inner tissues ofplants. E. coli O157:H7 migrated to internal locations in plant tissue and was thus protected from theaction of sanitizing agents by virtue of its inaccessibility. Experiments demonstrate that E. coliO157:H7 can enter the lettuce plant through the root system and migrate throughout the edible portionof the plant.” http://aem.asm.org/cgi/content/short/68/1/397

In the 2011 study, “Identification of the Cellular Location of Internalized Escherichia coli O157:H7 inMung Bean, Vigna radiata, by Immunocytochemical Techniques,” Amanda J Deering, et al., PurdueUniversity, said, “Escherichia coli O157:H7 has been associated with numerous outbreaks involvingfresh produce. Previous studies have shown that bacteria can be internalized within plant tissue and thatthis can be a source of protection from antimicrobial chemicals and environmental conditions.However, the types of tissue and cellular locations the bacteria occupy in the plant followinginternalization have not been addressed. In this study, immunocytochemical techniques were used tolocalize internalized E. coli O157:H7 expressing green fluorescent protein in germinated mung bean(Vigna radiata) hypocotyl tissue following contamination of intact seeds. An average of 13 bacteria permm(3) were localized within the sampled tissue. The bacteria were found to be associated with everymajor tissue and corresponding cell type (cortex, phloem, xylem, epidermis, and pith). The corticalcells located on the outside of the vascular bundles contained the majority of the internalized bacteria(61%). In addition, the bacteria were localized primarily to the spaces between the cells (apoplast) andnot within the cells. Growth experiments were also performed and demonstrated that mung bean plantscould support the replication of bacteria to high levels (10(7) CFU per plant) following seedcontamination and that these levels could be sustained over a 12-day period. Therefore, E. coliO157:H7 can be internalized in many different plant tissue types after a brief seed contamination event,and the bacteria are able to grow and persist within the plant.”http://www.mendeley.com/research/identification-cellular-location-internalized-escherichia-colio157h7-mung-bean-vigna-radiata-immunocytochemical-techniques/

In a Droffner and Brinton study (1995), "It was observed that Salmonella and E. coli survived for 59 days at about 60degrees C in an industrial compost." However, they reported, "The bacteria became undetectable after thetemperature decreased from 62 degrees C to about 40 degrees C in the compost curing."

The Bacillus coli communis, called also Bacterium coli commune, the colon bacillus, or the bacillus of Escherich was discovered in feces by Emmerich in 1885. Under ordinary conditions this is a putrefactive bacillus inhabiting the intestinal canal and feces invariable contains it. It is found in the mouth, nose, and vagina, on the skin, and under the nails. The bacillus is normally found in water, even in water regarded by users as pure. It has already been stated that this ordinarily harmless micro-organism may, under certain conditions, acquire pathogenic power and enter the circulation. This bacterium grows best in air, but it can also grow when air is excluded.

This bacillus may be responsible for appendicitis, peritonitis, inflammation of the genito-urinary tract, pneumonia, inflammation of the intestine, leptomeningitis, perineal abscess, cholangitis, cholecystitis, myelitis, puerperal fever, wound infections and septicemia. It is the cause of many abscesses about the intestine and responsible for many ischiorectal abscesses. From the pus of an appendicitis abscess we may perhaps obtain culture of Escherich's bacillus, but usually find also streptococci or staphylococci, and sometimes pneumococcus. Colon bacilli introduced into the system by tainted food may be responsible for epidemic pneumonia . A few years ago there was such an epidemic in Middlesbrough, England (Oliver, in "Brit. Med. Jour." April 30, 1910)

There is a misconception that E. coli in the body is harmless. Before you believe that you need to read the story of Lovella Thompson who loss her feet and is missing part of all 10 fingers because of E. coli that never got out of her body.

"Drug resistant genes are also inserted as markers in genetically engineered bacteria. Since there has been such a dramatic increase in drug resistant bacteria in the last 25 to 30 years, there is a common (scientific and public) theory that genetic engineers are responsible for a major portion of the increase. In fact, that theory may have some validity since a patent was assigned to Stanford University in 1980 for a process to insert genes into non-disease causing E. coli so as to create a bacteria never before seen in nature. Since that time E. coli has been the workhorse of genetic engineering." "It is an accepted "fact" that the use of antibiotics in humans and cattle create drug resistant bacteria. However, there is a caveat, a USDA investigation in 1982 did not find 0157:H7 in any cattle in the United States." "Scientists as well as EPA have known since the 50s that bacteria exchange DNA and genes in the treatment plant and spit out drug resistant bacteria in the sewage effluent water and are concentrated in the sewage biological solids in sludge."

It would apear that, "Sometimes prior to 1975, E. coli picked up a Shigella toxin gene unique to an epidemic in Central America. Only the toxins produced by tetanus and botulism are more dangerous. California researchers identified 20 cases of this unique strain of Shigella during 1969/70 in a retrospect study in 1972. The first E. coli 0157:H7 case (a Naval Officer) documented with samples at CDC was in Oakland, California in 1975. The Shigella like toxin (a known neurotoxin that produces delayed limb paralysis and death) was sequenced in 1986. It was noted that Escherichia coli of various serotypes, Salmonella typhimurium, and Vibrio choterae also produce the toxin. Researchers at Walter Reed Hospital had cloned the toxin producing gene by 1987."

Seventeen strains of H2S-producing variants of Escherichia coli were isolated from specimens submitted for microbiological study (ten from stool, five from urine, and two from postmortem material). Production of H2S was unstable in several strains; however, other than their production of H2S, all strains closely resembled typical E. coli in their biochemical reactions. In vitro susceptibilities of the H2S-producing variants to antimicrobics closely resembled those of typical E. coli in this laboratory.

The biochemical and serological characteristics of more than 200 H2S-positive variants of E. coli were recently reported by Darland and Davis (1).

1978An H2S-producing variant of Escherichia coli (strain 142) isolated from a urinary tract infection was found to be resistant to high levels of tetracycline, ampicillin, streptomycin, and sulfonamide. The H2S trait segregated spontaneously at a frequency of 2.5 x 10-3. No segregation was observed for the drug resistance determinants. Neither ethidium bromide nor acridine orange affected the rate of segregation of the drug resistance determinants or the trait for H2S production. Antibiotic resistance and hydrogen sulfide production were conjugally transferred to E. coli K-12 recipients at a frequency of approximately 1i-5 per donor cell. Antibiotic resistance and hydrogen sulfide production were also transduced as a single unit with phage P1L4. Genetic data, based on the segregation of resistance determinants and the H2S trait among transconjugant and transductant classes, suggested the presence of two R plasmids. Plasmid DNA was isolated by cesium chloride-ethidium bromide centrifugation. Two plasmid species were detected by agarose gel electrophoresis of purified plasmid DNA, a large molecule of about 80 x 106 daltons (designated pSR12) and a small molecular species of approximately 5.5 x 106 daltons (designated pSR13). Transformation studies using purified plasmid DNA showed that the large pSR12 plasmid confers resistance to ampicillin, tetracycline, and streptomycin and also carries the gene(s) for H2S production. The small pSR13 plasmid confers resistance to streptomycin and sulfonamide.------------------------------------------------------------------------------------------------------------------------------------------------Infections caused by ESBL-producing E. coli are a growing worldwide phenomenon and are not unique to the UK .The figure being quoted in the media of 30,000 cases of infection due to ESBL-producing E. coli each year in theUK is an estimate. The Health Protection Agency is one of the leading institutions worldwide in terms of research into this area and has been providing advice about these infections for many years and, in particular, produced a report on the increasing frequency of these infections in 2005.

The kinds of infections that ESBL-producing E. coli can cause range from urinary tract infections, to - at the moreserious end of the spectrum - cases where they enter the bloodstream and cause blood poisoning. Infections withESBL-producing E. coli are most common amongst the elderly, or those who have recently been in hospital orreceived antibiotic treatment. ESBL-producing E. coli are extremely rare in simple cystitis.http://deadlydeceit.com/E_coli-ESBL.html

Escherichia coli: (Coliform -- fecal coliform) E. coli is unique in that the most deadly bacteria 0157:H7only ferments lactose at 25°C (77°F) , while the coliform test is for bacteria that fermentlactose at 35°C (95°F ), and the fecal coliform test is for a thermotolerant E. coli bacteriathat ferments lactose at 44.5°C. (112.1°F)

"E. coli O157:H7 is markedly different from other pathogenic E. coli, as well. In particular, the O157:H7 serotype is negative for invasiveness (sereny test), elaborates no colonization factors (CFA/I or CFA/II), Doesn't produce heat stable or heat labile toxins and is non-hemolytic. In addition, E. coli O157:H7 is usually sorbitol negative whereas 93% of all E. coli ferment sorbitol.[6] E. coli O157:H7 also lacks the ability to hydrolyze 4-methylumbelliferyl-β-D-glucuronide (MUG)[7] and does not grow at 45 °C in the presence of 0.15% bile salts. Because of the latter characteristic this serotype cannot be isolated by using standard fecal coliform methods that include incubation at 45 °C.[7][8]"

The International Escherichia and Klebsiella Centre (WHO) has a very large strain collection of approximately 60,000 E. coli strains, most of which are clinical isolates. This collection includes test and reference strains for O, K, H and F antigens, various toxins and other E. coli virulence factors. The collection contains strains representing almost any possible sero- and virulence type.

The current public relation ploy is that because E. coli is a part of the normal gut flora it isnot harmful to humans. However, once E. coli leaves the gut it can be very deadly as in urinarytract infection or cause sepsis and meningitis in newborns.

0157:H7 can not be treated with drugs, antibiotic-resistant.Sequelae of ETEC, EPEC, and EIEC infection are not well described. Enteroaggregative E.coli may cause chronic diarrhea. There is no formal surveillance system for diarrheogenicE. coli and most laboratories are unable to identify them.Causes clinical mastitis in cattle.-----------------------------------------------------------------------------------------------------------------------------Genome Project Information for a few E. coli strains

Outbreaks of enterohemorrhagic Escherichia coli O157:H7 infections associated with lettuce and other leaf crops have occurred with increasing frequency in recent years. Contaminated manure and polluted irrigation water are probable vehicles for the pathogen in many outbreaks. In this study, the occurrence and persistence of E. coli O157:H7 in soil fertilized with contaminated poultry or bovine manure composts or treated with contaminated irrigation water and on lettuce and parsley grown on these soils under natural environmental conditions was determined. Twenty-five plots, each 1.8 by 4.6 m, were used for each crop, with five treatments (one without compost, three with each of the three composts, and one without compost but treated with contaminated water) and five replication plots for each treatment. Three different types of compost, PM-5 (poultry manure compost), 338 (dairy manure compost), and NVIRO-4 (alkaline-stabilized dairy manure compost), and irrigation water were inoculated with an avirulent strain of E. coli O157:H7. Pathogen concentrations were 107 CFU/g of compost and 105 CFU/ml of water. Contaminated compost was applied to soil in the field as a strip at 4.5 metric tons per hectare on the day before lettuce and parsley seedlings were transplanted in late October 2002. Contaminated irrigation water was applied only once on the plants as a treatment in five plots for each crop at the rate of 2 liters per plot 3 weeks after the seedlings were transplanted. E. coli O157:H7 persisted for 154 to 217 days in soils amended with contaminated composts and was detected on lettuce and parsley for up to 77 and 177 days, respectively, after seedlings were planted. Very little difference was observed in E. coli O157:H7 persistence based on compost type alone. E. coli O157:H7 persisted longer (by >60 days) in soil covered with parsley plants than in soil from lettuce plots, which were bare after lettuce was harvested. In all cases, E. coli O157:H7 in soil, regardless of source or crop type, persisted for >5 months after application of contaminated compost or irrigation water.

Enterohemorrhagic Escherichia coli (EHEC) pathogenicity is usually linked to a Shiga toxin (1,2) and virulence factors, including adhesins, toxins, invasins, protein secretion systems, iron uptake systems, and several unidentified functions (3,4), which are unrelated to strain phylogeny. In many laboratories, sorbitol-MacConkey medium is commonly used to screen for the slow sorbitol fermentation phenotype of the most common Shiga toxin–containing strain: O157:H7 (5), but this process does not address the pathogenic potential of the remaining sorbitol-positive E. coli. These organisms can be detected by immunologic methods or PCR evaluation of virulence factors. PCR is the most useful method for virulence factor detection, and others have made convincing arguments for its use in characterizing the virulence factor patterns of potential pathogens (6,7).

Variation in virulence factor targets and use of different PCR primers contribute to variable results in detecting the most common virulence factors: stx1, stx2, eae, and hlyA (or ehxA). Variation in amplification success is likely to increase because more virulence factor variants are certain to emerge as more EHEC and Shiga toxin–producing E. coli (STEC) strains are identified. This study addresses the potential for a broad and well-characterized set of control strains relative to virulence factor amplification and confirmed by Southern hybridization.---------------------------------------------------------------------------------------------------------------------------------------------It is EPA's contention that E. coli only cause:

2. Escherichia coli (pathogenic strains): ---------Gastroenteritis.

The Cytotoxic Necrotizing Factors (2007) from Yersinia pseudotuberculosis and from Escherichia coli Bind to Different Cellular Receptors but Take the Same Route to the Cytosol

The pathogenic groups includes enterotoxigenic E. coli (ETEC), enteropathogenic E. coli (EPEC), enterohemorrhagic E. coli . ETEC may produce a heat-labile enterotoxin (LT) that is very similar in size (86 kDa), sequence, antigenicity, and function to the cholera toxin (CT). EIEC closely resemble Shigella and causes an invasive, dysenteric form of diarrhea in humans (6). Like Shigella, there are no known animal reservoirs; hence the primary source for EIEC appears to be infected humans. Pathogenicity of EIEC is primarily due its ability to invade and destroy colonic tissue. EPEC causes a profuse watery diarrheal disease and it is a leading cause of infantile diarrhea in developing countries. EHEC are recognized as the primary cause of hemorrhagic colitis (HC) or bloody diarrhea, which can progress to the potentially fatal hemolytic uremic syndrome (HUS). The infectious dose for O157:H7 is estimated to be 10 - 100 cells; but no information is available for other EHEC serotypes.http://www.cfsan.fda.gov/~ebam/bam-4a.html

One of the group of Enterobacteriaceae which includes: Enterobacter, Escherichia, Klebsiella, Morganella, Proteus, Providencia, Salmonella, Serratia, Shigella, and Yersinia.

Bloody, watery, or inflammatory diarrhea (traveler's diarrhea). In children, diarrhea caused by certain strains of E. coli may lead to destruction of red blood cells and kidney failure (hemolytic-uremic syndrome). E. coli can also cause urinary tract infections (particularly in women) and bacteremia and meningitis in newborns (particularly premature newborns). May cause severe, lung infection , pneumonia, may lead to the formation of abscesses (collections of pus) in the lung or in the lining of the lungs (empyema).may cause deep infections, particularly in the urinary tract and the abdominal cavity. (Merck)

AbstractThree strains of Escherichia coliO157:H7 (ATCC 43895, Ent C9490 and 380–94) were inoculated into salami and heated in water baths at 50, 55 or 60°C. At intervals between 1 and 360 min, salami samples were removed from the water bath and examined for the presence of survivingE. coliO157:H7. Samples were directly plated onto sorbitol MacConkey (SMAC) agar, and onto tryptone soya agar (TSA) with SMAC overlay. The number of sub-lethally damaged cells in each sample was estimated from the differences between the resultant direct (uninjured cells only) and overlay (total recovery) counts. In samples heated at 50°C, the percentage of cell injury ranged from 71·8–88% for all strains. In samples heated at 55°C the percentage of sub-lethally damaged cells in strains ATCC 43895 and Ent C9490 was significantly higher (P< 0·001) at 97% than that observed in strain 380–94 (64%). Cell injury was not measured at 60°C. There were significant differences between the derived decimal reduction times (D-values) related to the different strains ofE. coliO157:H7, the heat treatment applied and the recovery/enumeration agars used. Significant interstrain differences (P< 0·05) in thermotolerance were noted. Strain Ent C9490 was significantly more heat resistant at 50°C and 60°C (D-values of 116·9 and 2·2 min, respectively), while at 55°C strain 380–94 was more thermotolerant (D-value of 21·9 min). The implications of these findings for the design of studies investigating the heat resistance ofE. coliO157:H7 in fermented meat environments are discussed.

*1 Portions of this research were presented at the Annual Meeting of the International Association of Milk, Food, and Environmental Sanitarians, 30 June to 3 July 1996 in Seattle, Washington, USA.

Mention of brand or firm names does not constitute an endorsement by the US Department of Agriculture over others of a similar nature not mentioned.

Preventing the spread of all types of verocytotoxin-producing E.coli(VTEC) meat depends not so much on the temperature at which you storeit, but rather the temperature at which you cook it.

According to the Mustafa Khammash at the University of California atSanta Barbara the ideal temperature for the growth of E.coli is 37Celsius. You can check out a Power Point Presentation of his study ofthe Feedback Regulation of Bacterial Stress Response at:www.engineering.ucsb.edu/~mdsymp/ppt/khammash.pptThere's a chart on the fourth page down.

According to the Insitute of Food Science and Technology temperaturesbelow -5 degrees Celsius may retard the growth of E.Coli, but theorganism will survive.

From http://www.ifst.org/hottop1.htm"Refrigeration below 5 deg C is thought to prevent growth of VTEC andis an important hygiene measure. However, any organisms present arelikely to survive at these temperatures perhaps for several weeks."

The key to killing E.coli in meat is to thoroughly cook it at atemperature of 68.3 Celsius (approx. 160 F) or higher, for at leasttwo minutes.

AnimalsColibacillosis occurs as an acute fatal septicemia or subacute pericarditis and airsacculitis. It is a common systemic disease of economic importance in poultry and is seen worldwide.

Baby Calf Health: Common Diarrheal DiseasesColibacillosis - E. coli - Colibacillosis usually occurs in calves 1-10 days old. Typically, calves out of first calf heifers are more susceptible. Other associated factors include seasonal variation, overcrowding and poor sanitation which allow build up of organisms in calving pens. Milk pails and feeding equipment can become contaminated. Signs include frequent and effortless diarrhea, pasted rear quarters, fluid or semisolid malodorous feces with chunks of partially digested milk, rapid dehydration and weight loss, depression, anorexia, weakness, and death. Body temperature is normal at first but subnormal as the disease worsens. Death can occur in 3-5 days. Mixed infections can occur along with rota/corona virus and/or cryptosporidiosis. Illness can occur in up to 75 percent of calves on a farm, while death losses can range from 10 to 50 percent in unvaccinated herds.

Disease prevention is primarily achieved by early, rapid ingestion of colostral antibodies. Hours matter. A recent study showed that if colostrum was given 3 hours after infection with E. coli, the calves were protected against disease. If colostrum consumption was delayed until 4 hours after infection up to 40 percent of the calves died. All calves became ill if colostrum was given 5 hours after infection. E. coli bacterins used to prevent calf diarrhea are different from E. coli mastitis bacterins. Monoclonal antibodies work if given early (immediately after birth). Antibodies against E. coli antigens have little effect once the diarrhea has commenced, they are principally prophylactic.